HYPONATREMIA & HYPERNATREMIA

1. HYPONATREMIA&HYPERNATREMIA DR. HAMED SHAKHATREH NEPHROLOGIST CONSULTANT

2. HYPONATREMIA • Normal S. Sodium 135-148 mmol/L • <135 = 22% of hospital patients • <130 = 4% of hospital patient • Hyponatremia important because: • Acute hyponatremia cause morbidity & mortality • Mild hyponatremia can progress to severe during treatment • Rapid correction can produce severe neurological deficits and death. • Hyponatremiaand hypoosmolality are usually synonymous because the calculated osmolality. • P osm = 2 Na + glucose mmol/L + BUN mmol/L

3. The normal range 275- 295 • Hyponatremia = hypoosmolality except in 3 conditions: • High proteins • High glucose • High Lipids • Here the hyponatremia called pseudohyponatremia because the true sodium is normal if it measure by ion specific electrode not by photometry. • For example: S. glucose 500mg/dl • & S. Na 125mmol/L • The true Na= 125 + (4x2.4) =135 mmol/L

4. PATHOGENESIS: • Depletion (primary decrease in total body solute + secondary water retention) • Renal solute loss • Diuretic use • Solute diuresis (Glucose, Mannitol) • Solute wasting nephopathy • Mineralocorticoid deficiency • Non renal solute loss • Gastro intestinal (diarrhea, vomiting, pancreatitis, bowel obstruction) • Cutaneous (sweating, burns) • Blood Loss

5. Dilution (primary increase in total body water + secondary solute depletion). • Impaired renal free water excretion • Increased proximal reabsorption • Hypothyroidism • Impaired distal dilution • SIAD • Glucocorticoid deficiency • Combined increased proximal reabsorption and impaired distal dilution • CHF • Cirrhosis • Nephrotic syndrome • Decreased Urinary solute excretion • Beer Potomania • Excess water intake • Primary polydipsia • Dilute infant formula

6. Differential Diagnosis: • Decreased volume (hypovolemia) 20% orthostatic changes • Decreased urine sodium <30 non renal cause: G/E • Increase urine Na >30 renal cause • Diuretic the most common cause & Thiazide the common. • Low S.K indicate hypovolemia • Chronic interstitial nephropathy • PKD, Bartter’s Syndrome, Addison’s Disease.

7. EUVOLEMIA 33% • Bp & Ps without orthostatic changes BUN & Uric Acid normal or low urine sodium <30 unlikely due to primary dilutional except in hypothyroidism. • While Urine Na >30 = SIAD

8. Criteria to Diagnose SIAD:Essential: • Decreased osmolality P. <275 • Inappropriate urine osmolality urine >100mo/kg. H2O with S. hypoosmolality • Clinical Euvolemia • Increased urine Na on normal salt & water intake • Absence of causes of hypoosmolality such hypothyroidism, Addison’s disease and diuretics.

9. SUPPLEMENTAL: • Abnormal water load 20ml/kg over 4 hours. Failure to dilute U osm <100 • AVP inappropriately elevated relative to plasma hypo osmolality. • S. Na improved with water restriction but not with volume expansion.

10. COMMON CAUSES OF SIAD • Tumors • Pulmonary, GIT, Prostate Uterine Leukemia • Central NS disorders • Tumors, Abscess encephalitis, Meningitis • Drug Induced • Stimulated • Nicotine, Phenothiazine • Tricyclics and others • Pulmonary Disease • TB, Aspergillosis, COPD

11. Increased ECF (Edema & Ascites 35%) • Clinical edema or ascites • Na <30 mmol • Sometimes Na >30 mmol/L because of glucosuria, diuretic theraphy. • Hyponatremia usually in advanced disease as CHF, Nephrotic syndrome and Cirrhosis.

12. CLINICAL MANIFESTATION • Clinical picture depends on severity, speed of hyponatremia which means more than 48 hours or less. • The picture reflect brain edema which presented from confusion to seizures to coma and the comorbilities. • Special high incidence of morbidity & mortality in menstruating females & young children specially post operative.

13. THERAPY • Theraphy depends on severity of clinical situations, the level of S. Na, the period of which hyponatremia happened less than 48 hours or longer. • Any correction not allowed more than 12 mmol/L in any 24 hours. • Safe level >120 restrict water. • Rapid correction induced pontine & extra poutinemyelinolysis.

14. How to correct hyponatremia • (infusate- actual)% (BW/2+1) or hypertonic saline 3%- 70ml/hr in 70kg patient increase S. Na by 1. • SIAD – Demeclocyline 600mgx2 to induce NDI. • Phenytoin, Opiates, Ethanol- decreased AVP.

15. HYPERNATREMIA • Decreased in total body water, however total body Sodium maybe normal, increased or decreased. • Hypernatremia happened in 2% of patients. • Hypernatremia presented in two ways: • Pre- Hospital or Intra-hospital.

16. REGULATION OF WATER HOMOESTASIS: • This happened by the interaction of AVP in the Hypothalamus through posterior pituitary gland & the thirst centre in the anterior wall of third ventricle with the distal collecting duct in the kidney. Osmostat in the hypothaleum proportionally affected by osmolality decreased osmolality decreased AVP. • Thirst center regulated with 5 mml/kg above osmostat.

17. PATHOPHYSIOLOGY: • Hypernatremia happened with thirst sense lost or unable to get water. • Defects in Thirst: • Primary- Hypodypsia • Hypothalamic lesion • Trauma • Craniopharyngioma or Supracellular Tumor • Metastatic Tumor • Granulomas • Vascular Lesion • Essential Hypernatremia • Geriatric Hypodypsia

18. Secondary- Cerebravascular Disease • Dementia • Delirium • Mental Status Changes

19. CLINICAL MANIFESTATION: • Picture of hypernatremia mostly neurological and appear as confusion, seizures up to coma due to brain shrinkage & dehydration and also depends on the speed of appearance and state of hyperosmolality.

20. CLINICAL CLASSIFICATION: • Classifications according to changes in extra cellular volume. • Pure Water Deficit • DI – hypothalamic • Nephrogenic • Hypotenic Fluid Loss • Renal • GastroIntestinal • Cutaneous • Hypertonic Sodium Gain • Salt Ingestion • Hypertonic Sodium Chloride • Hypertonic Sodium Bicarbonate • Total parenteral nutrition

21. Hypothalamic DI Nephrogenic DI • - Pituitary Surgery - Drug Induced • - Head Traum Lithium • - NeoplasiaDemeclocycline • - Vascular Lesion Amphotrecin B • Sheehan’s syndrome - Electrolyte disturb • - Infection Hypercalcemia • - GranulomasHypokalemia • - Autoimmune - Obstructive uropathy - Congenital X-linked

22. TREATMENT • The treatment of hypernatremia is water. • Water deficit = 0.6 BW (Na/140-1) • Rapid correction not allowed only 0.5 mmol/L S. Na reduced in hour. • Rapid correction cause intra cranial hemorrhage • CDI- treated by AVP • NDI- treated by Thiazide • Amiloride • If hypernatremia with overload & comorbidity such as renal failure- hemodialysis is necessary.